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At least 19 recordsLinked to original sources
PubMed2000

From biological clock to biological rhythms.

The genetic and molecular analysis of circadian timekeeping mechanisms has accelerated as a result of the increasing volume of genomic markers and nucleotide sequence information. Completion of whole genome sequences and the use of differential gene expression technology will hasten the discovery of the clock output pathways that control diverse rhythmic phenomena.

Animals↗
PubMed2006

Constant light disrupts the developing mouse biological clock.

The central biological clock of the brain, contained within the suprachiasmatic nuclei (SCN) of mammals, orchestrates an orderly "internal day" of physiology and behavior. The developing biological clock begins to respond to light at an early stage and a particular concern in humans is whether light exposure has disruptive effects on the developing biological clock of infants exposed to constant lighting conditions in neonatal intensive care units (NICUs). Worldwide, eighteen million, or 14%, of newborns estimated to be of low birth weight, are exposed to artificial lighting environments in hospital nurseries annually. Here, we have tested whether constant light (LL) exposure disrupts the developing biological clock of mice, using a circadian reporter transgenic mouse model in which the organization of the central biological clock can be assayed by real-time gene expression imaging. We now find that LL has both acute and long-term disruptive effects on developing biological clocks and that cyclic lighting conditions are critical for developing circadian clocks to coordinate their molecular circadian mechanisms. This suggests that, from the perspective of developing circadian organization in humans, cyclic light conditions in NICUs are likely to be most appropriate for infants.

Animals↗
PubMed2006

The male biological clock.

Do men have biological clocks that affect their hormone levels, fertility, and the genetic quality of their sperm? Women can no longer be viewed as solely responsible for age-related fertility and genetic problems. The effects of andropause and advanced paternal age on fertility and offspring are still under investigation. Further research is needed to fully characterize the associated risks and to treat the underlying abnormalities. A better understanding of the cellular and biochemical mechanisms of "gonadal" aging is important in order to determine safe, effective ways to delay this process and "rewind" the male biological clock. The benefits may include decreasing the potential for adverse genetic consequences in offspring, improvement in the sexual and reproductive health of aging males, and increase a woman's chance of having healthy children by correcting defects in the male reproductive system.

Aging↗
PubMed2006

[The biological clock in health and illness].

The biological clock in mammals is located in the suprachiasmatic nuclei of the hypothalamus. The combined output of multiple neuronal cellular oscillators determines the master circadian rhythm, which paces the myriad periodic functions of the organism, including, to a certain degree, the sleep-wake rhythm. The intrinsic master circadian rhythm, which is slightly longer than 24 hours, is synchronized daily to the extrinsic 24-hour day by the entrainment process, governed mainly by exposure to the environmental light at specific times. The pineal hormone melatonin is a specific and sensitive marker of the circadian clock activity, and its secretion is tightly coupled to the output of the biological clock and the circadian phase. Chronobiology is a young scientific discipline which deals with research of the biological clocks and its implication to the clinical medicine. Circadian rhythm disorders are manifest mainly as inappropriate sleep-wake timing, and patients complain about various combinations of insomnia or excessive sleepiness at inappropriate times. Treatment of circadian rhythm disorders by sleeping pills or wake-promoting agents, without taking chronobiological considerations into account, may be futile, or even detrimental to a patient's well-being. The current issue of "Harefuah" includes a review by Doljansky and Dagan, which exemplifies the chronobiological approach to sleep-wake rhythm disturbances in patients with Alzheimer's disease. Adoption of this approach to other disorders of the circadian clock may benefit care of patients.

Biological Clocks↗
PubMed1999

Biological clocks.

Circadian rhythms describe biological phenomena that oscillate with an approximately 24-hour cycle. These rhythms include blood pressure, body temperature, hormone levels, the number of immune cells in blood, and the sleep-wake cycle. In this paper, we will focus on common genes between species that are responsible for determining the circadian behavior, especially some transcription factors (i.e., switch genes) that serve to regulate many circadian rhythm genes. The intent of this summary is to introduce the common molecular mechanism of biological clocks between flies and humans and then to describe the research from three laboratories that was presented in the session.

Animals↗
PubMed1987

Molecular mapping of point mutations in the period gene that stop or speed up biological clocks in Drosophila melanogaster.

The pero1 and the pers mutations in Drosophila melanogaster, which seem to eliminate or speed up, respectively, the clocks underlying biological rhythmicity, were mapped to single nucleotides. Chimeric DNA fragments consisting of well-defined wild-type plus mutant DNA subsegments were constructed, introduced into flies by germ-line transformation, and assayed for biological activity. These experiments localized both pero1 and pers to a 1.7-kilobase DNA fragment that is mostly coding DNA. Sequencing of this subsegment from each mutant showed that pero1 is completely accounted for by a nonsense mutation in the third coding exon of a 4.5-kilobase RNA transcribed from this locus. The pers mutation is also a single nucleotide substitution, in the fourth coding exon, which results in a serine-to-asparagine substitution in the per gene protein product. The functional significance of these changes is discussed with reference to the phenotypes of the two mutations.

Amino Acid Sequence↗
PubMed2002

Melanopsin: a novel photopigment involved in the photoentrainment of the brain's biological clock?

The brain's biological clock located in the suprachiasmatic nucleus (SCN) generates circadian rhythms of physiology and behaviour of approximately 24 hours. The clock needs, however, like a watch that runs too fast or too slow, daily adjustment and the most important stimulus for this adjustment is the environmental light/dark cycle, a process know as photoentrainment. It is well established that the eye contains a separate anatomical and functional system mediating light information to the clock. Until recently, the photopigment responsible for light entrainment of the circadian system has been elusive but recent studies have provided evidence that melanopsin, a recently identified opsin, could be the circadian photopigment. This conclusion is based on the observation that melanopsin is expressed exclusively in retinal ganglion cells projecting to the SCN, a projection known as the retinohypothalamic tract (RHT) and that these ganglion cells are intrinsically photosensitive. Melanopsin is present in the plasma membrane of soma, dendrites and axons forming an extensive photoreceptive network in the entire retina. Although these findings make melanopsin a strong candidate as a circadian photopigment, a number of functional experiments are needed before the role of melanopsin is finally proven.

Animals↗
PubMed1992

Pre-natal development of a hypothalamic biological clock.

The available evidence indicates that a biological clock oscillates in the mammalian fetus and that the fetal clock is entrained by redundant circadian signals from the mother. An entrainable biological clock during fetal life helps the developing mammal more readily prepare for life in the outside world. In humans, the early establishment of maternal-infant synchrony may help the infant maximize its responsiveness to the outside world.

Animals↗
PubMed2006

Rethinking the biological clock: eleventh-hour moms, miracle moms and meanings of age-related infertility.

Over the past generation, aging and female reproduction have been lodged within the gendered and gendering debates regarding women's involvement in the workforce and demographic shifts toward delayed parenting that culminate in discourses on the "biological clock". Technological solutions to the biological clock, specifically in vitro fertilization, have led to clinical attempts to assess "ovarian reserve", or qualitative and quantitative changes in the ovary that correlate with aging and with successful infertility treatment. Rupturing the longstanding historical connections between menstruation and female reproductive capacity by specifically focusing on the aging of a woman's eggs, the clinical designation of "diminished ovarian reserve" has come to imply that a woman has "old eggs". This is associated in practitioners' and patients' minds with the eclipse of a woman's reproductive potential and with hidden harbingers of menopause. In an ethnographic interview study of 79 couples in the US who conceived after using donor oocytes, we found that women voiced two different narratives that described their experience and attitudes when confronted with an apparent age-related decline in their fertility. The "eleventh-hour mom" narrative was voiced by women who initially tried to become pregnant with their own eggs and turned to donated oocytes as a second-choice option, whereas the "miracle mom" narrative was expressed by women who were generally older, some of whom had entered infertility treatment hoping to conceive with their own eggs, but some who knew from the outset that it was not going to be possible. Through their narratives women not only embodied and made meaningful "diminished ovarian reserve" in varying ways that connect with cultural, social, structural/organizational, symbolic and physical aspects of aging, they reproduced the socio-biological project of the biological clock, but rooted this social project in the metaphor of "old eggs" rather than menopause.

Adult↗
PubMed2001

Spatiotemporal variation of metabolism in a plant circadian rhythm: the biological clock as an assembly of coupled individual oscillators.

The complex dynamic properties of biological timing in organisms remain a central enigma in biology despite the increasingly precise genetic characterization of oscillating units and their components. Although attempts to obtain the time constants from oscillations of gene activity and biochemical units have led to substantial progress, we are still far from a full molecular understanding of endogenous rhythmicity and the physiological manifestations of biological clocks. Applications of nonlinear dynamics have revolutionized thinking in physics and in biomedical and life sciences research, and spatiotemporal considerations are now advancing our understanding of development and rhythmicity. Here we show that the well known circadian rhythm of a metabolic cycle in a higher plant, namely the crassulacean acid metabolism mode of photosynthesis, is expressed as dynamic patterns of independently initiated variations in photosynthetic efficiency (phi(PSII)) over a single leaf. Noninvasive highly sensitive chlorophyll fluorescence imaging reveals randomly initiated patches of varying phi(PSII) that are propagated within minutes to hours in wave fronts, forming dynamically expanding and contracting clusters and clearly dephased regions of phi(PSII). Thus, this biological clock is a spatiotemporal product of many weakly coupled individual oscillators, defined by the metabolic constraints of crassulacean acid metabolism. The oscillators operate independently in space and time as a consequence of the dynamics of metabolic pools and limitations of CO(2) diffusion between tightly packed cells.

Biological Clocks↗
PubMed2002

Chronopathological forms of magnesium depletion with hypofunction or with hyperfunction of the biological clock.

The main mechanisms of the chronopathological forms of magnesium depletion associate a low Mg intake with various dysregulating biorhythms. The differentiation between forms with hyperfunction and forms with hypofunction of the biological clock is seminal and the main marker is the production of melatonin (MT). The clinical forms of the various patterns of the chronopathological forms of Mg depletion may be central or peripheral. The clinical forms with hyperfunction of the biological clock (marker: increase in MT) may associate diverse expressions of nervous hypoexcitability: depression (i.e. Seasonal affective disease); cephalalgias nocturnal, without photophobia (i.e. cluster headaches); dyssomnia LASPS (advanced sleep phase syndrome) particularly]; asthenia and myalgias (i.e. fibromyalgia, chronic fatigue syndrome). The main comorbidity is found with depressive states. The therapy relies on classical bright light phototherapy, sometimes associated with psychoanaleptics. The clinical forms with hypofunction of biological clock (marker: decrease in MT) may associate various signs of nervous hyperexcitability (HEN): anxiety (from generalized anxiety to panic attacks); cephalalgias diurnal with photophobia (mainly migraine); dyssomnia [DSPS (delayed sleep phase syndrome) particularly, jet lag, night work disorders, age related insomnia, sometimes with inappropriate behaviour; photogenic epilepsia, generalized or focal; some clinical forms of chronic fatigue syndrome and fibromyalgia. The main comorbidity is between migraine and epilepsia. The treatment relies on the diverse forms of darkness therapy, possibly with the help of some psycholeptics: anxiolytics and anticonvulsants. The indications of chromatotherapy remain to be validated.

Animals↗
PubMed1990

The quail's eye: a biological clock.

The site (intraocular vs. extraocular) of the biological clock driving a rhythm in melatonin content in the eyes of Japanese quail was investigated by alternately patching the left and right eyes of individual birds, otherwise held in constant light, for 12-hr periods. This patching protocol, therefore, exposed each eye to a light-dark cycle (LD 12:12) 180 degrees (12 hr) out of phase with the LD cycle experienced by the other eye. The optic nerves to both eyes were transected prior to initiating the patching protocol. The ocular melatonin rhythm (OMR) of the left eyes of quail could be entrained by this procedure 180 degrees out of phase with the rhythm expressed by the right eyes. Since optic nerve section would have deprived any putative extraocular clocks of photic entrainment information, the results show conclusively that the clock driving the OMR is located within the eye itself. In addition, the OMR of Japanese quail is remarkably unaffected by removing two potential neural inputs to the eye (sympathetic innervation from the superior cervical ganglia, and input from the isthmo-optic nucleus of the midbrain); this suggests that these inputs are not required to maintain the OMR. Finally, the clock driving the OMR of one eye does not appear to be coupled to the clock driving the OMR in the other eye, since permanently patching one eye abolished the ability of the patched eye to re-entrain to an 8-hr shift in the phase of an LD 12:12 cycle, whereas the exposed eye rapidly re-entrained to the phase-shifted cycle.

Animals↗
PubMed1997

Localization and characterization of nitric oxide synthase in the rat suprachiasmatic nucleus: evidence for a nitrergic plexus in the biological clock.

Behavioral and electrophysiological evidence indicates that the biological clock in the hypothalamic suprachiasmatic nuclei (SCN) can be reset at night through release of glutamate from the retinohypothalamic tract and subsequent activation of nitric oxide synthase (NOS). However, previous studies using NADPH-diaphorase staining or immunocytochemistry to localize NOS found either no or only a few positive cells in the SCN. By monitoring conversion of L-[3H]arginine to L-[3H]-citrulline, this study demonstrates that extracts of SCN tissue exhibit NOS specific activity comparable to that of rat cerebellum. The enzymatic reaction requires the presence of NADPH and is Ca2+/calmodulin-dependent. To distinguish the neuronal isoform (nNOS; type I) from the endothelial isoform (type III), the enzyme activity was assayed over a range of pH values. The optimal pH for the reaction was 6.7, a characteristic value for nNOS. No difference in nNOS levels was seen between SCN collected in day versus night, either by western blot or by enzyme activity measurement. Confocal microscopy revealed for the first time a dense plexus of cell processes stained for nNOS. These data demonstrate that neuronal fibers within the rat SCN express abundant nNOS and that the level of the enzyme does not vary temporally. The distribution and quantity of nNOS support a prominent regulatory role for this nitrergic component in the SCN.

Animals↗